Recent experiments on brain circuits in the monkey brain have mapped out a pathway that extends from the brainstem to the frontal lobe of cerebral cortex. This pathway carries what is referred to as a corollary discharge signal, that is, a copy of the neuronal activity that is going to be directed to the muscles in order to produce a movement. The copy or corollary discharge is not used to produce the movement but instead is used to inform other regions of the brain that this movement is about to occur. Thus this circuit in the monkey serves to monitor on-going movements and convey that information to the frontal lobe. This has been conclusively demonstrated by showing that a type of saccadic eye movement in the monkey, which depends on a corollary discharge, is disrupted when the corollary discharge pathway is inactivated. A well known hypothesis on the underlying mechanisms of a number of deficits observed in schizoprenia has been based on the concept of a corollary discharge. Specifically, the hypothesis is that in schizophrenia there is a disruption of the corollary discharge that could impair the self-monitoring of thoughts or actions. A consequence of this is that these thoughts or actions are not recognized as being generated by the patient and are therefore misattributed to external sources. Such corollary discharge deficits in schizophrenia could arise from the disrupted subcortical input to cortical circuits, disruptions that are known to characterize the disease. In addition it has been shown that patients with schizophrenia are impaired in tasks requiring corollary discharge and their auditory systems show particularly strong evidence for loss of corollary discharge-related modulation. While a contribution of impaired corollary discharge to schizophrenic positive symptoms, e.g. hallucinations, is the most obvious tie-in of the function to the disease, it has been argued that impaired corollary discharge could contribute to negative and cognitive symptoms as well. The objective or this study is to note if there is a defect in internal monitoring of eye movements in patients with schizophrenia. Both normal and schizophrenic subjects are asked to follow jumping target lights as their eye movements are monitored. The target lights are shown for brief periods and then extinguished before any eye movements are made, i.e. remembered targets. In one task a sequence of lights are shown and subjects are asked to move their eyes to the locations of the remembered sequence in the dark. In this way we are able to look for evidence of a defect in spatial location updating in subjects with schizophrenia. Four normal volunteers have been recruited and tested. Schizophrenic subjects are currently being recruited. No results have been obtained to date.